The invention generally relates to systems and methods for treating seizures and, in particular, to a method of cooling the cortex using a Peltier cell to abort intractable focal neocortical epilepsy.
Well over half of the resections for the treatment of intractable seizures are directed at temporal lobe epilepsy (1). In Olivier's series of 560 operations for control of epilepsy, 74% were on temporal lobes, 11% on frontal lobes, 1.3% on central regions, 0.9% on parietal lobes, and 0.8% on occipital lobes (2). The other 12% were multilobar resections (2.5%) and corpus callosotomies (9.5%). This may be related to the relatively high epileptogenicity of the mammalian temporal lobe, but may also reflect the greater ease in localizing and resecting epileptic foci in the temporal lobes (3). The surgical therapy of intractable neocortical epilepsy is still suboptimal for many children and adults. There are at least three reasons for this. First, it can be difficult to identify the exact site(s) responsible for seizure generation. Second, the extent of the required resection is not easy to anticipate. Third, removal of the seizure focus might produce an irreversible neurological deficit not predicted from presurgical neuropsychological or radiological evaluation. The complexity of functional localization is especially serious in children, who cannot undergo direct cortical mapping under local anesthesia (4).
We have, therefore, become interested in exploring alternative techniques to address these problems related to the surgical therapy of the neocortical epilepsies. We were aware of a substantial literature in neurophysiology and experimental neurology documenting the ability of focal cooling to reversibly inactivate the mammalian cortex (5, 6). We have also reviewed earlier research demonstrating that focal cooling can diminish paroxysmal activity in vivo (7, 8, 9).
In particular, we have become interested in exploring the possibility that focal cooling might enhance the surgical therapy of neocortical epilepsy. There is already a substantial literature in neurophysiology and experimental neurology demonstrating the ability of cooling to reversibly inactivate the central nervous system103,104. The precise mechanism(s) mediating the functional effects of cooling are not fully understood, but in vitro cellular reports have demonstrated that cooling can interfere with normal synaptic transmission and voltage-gated ion channels105,106,107.
Clinicians have recognized a relationship between seizures and temperature for centuries and there are a few modern accounts of terminating seizures in patients by temperature reduction108,109. There are also several in vivo and in vitro studies demonstrating a slow reduction in paroxysmal activity in models of epilepsy after gradual cooling110,111,112,113. The ready availability of small thermoelectric (Peltier) cooling devices, initially developed for the computer industry, makes cortical cooling an especially attractive option for investigation (see FIG. 9A, below)114.